Preparatory Mindset
AKI is a RAPID decline in kidney function over hours to days. The three categories (pre-renal, intra-renal, post-renal) guide diagnosis and treatment. Pre-renal = decreased perfusion (BUN:Cr >20), intra-renal = direct damage (ATN most common), post-renal = obstruction (USG shows hydronephrosis). Urine electrolytes help distinguish pre-renal from ATN.
Core Concepts
- AKI = rapid ↓ in GFR over hours-days → ↑ Cr and BUN.
- Pre-renal: ↓ renal perfusion (dehydration, heart failure, hemorrhage).
- Lab: BUN:Cr >20, FeNa <1%, urine osmolality >500.
- Intra-renal: direct kidney damage.
- ATN most common (ischemic or nephrotoxic).
- Lab: BUN:Cr <15, FeNa >2%, muddy brown casts in urine.
- Post-renal: obstruction (stones, prostate, tumor).
- USG shows hydronephrosis.
- Complications: hyperkalemia (most immediately dangerous), metabolic acidosis, fluid overload, uremia..
High-Yield Points
- BUN:Cr ratio >20:1 → pre-renal; <15:1 → intra-renal
- FeNa <1% → pre-renal; >2% → ATN (intra-renal)
- ATN: most common cause of intra-renal AKI
- Phases: oliguric → diuretic → recovery
- RIFLE/AKIN criteria for staging severity
Topic Summary
AKI is classified as pre-renal (hypoperfusion), intra-renal (direct kidney damage — ATN most common), or post-renal (obstruction). Treatment addresses the underlying cause and prevents complications.